JOINT DISORDERS AND REHABILITATION PST 427 OSTEOARTHRITIS (Part 1): Classification, Aetiology, Pathology and Clinical Features REVIEW OF SYNOVIAL JOINTS- Anatomy and Physiology • Articular surfaces are covered with hyaline cartilage • Joint capsule and ligaments unite the bones, provide stability and direct movement • Synovial membrane lines the capsule and secretes synovial fluid • Intra-articular structures are present in some joints such as menisci and cartilaginous discs • Nerve supply is from the nerves that supply the muscles acting on the joints (Hilton’s law) • Nerve endings in the capsule and ligaments are mechanoreceptors- to register movt, proprioceptors- to register joint position, and nociceptors- to register pain. There are also autonomic (sympathetic) nerve endings on blood vessels. OSTEOARTHRITIS • It is defined as a chronic degenerative dx of joints with exacerbations of acute inflammation. • Osteoarthritis is 'morphologic, biochemical, molecular and biochemical changes of both cells and matrix which lead to softening, fibrillation, ulceration and loss of articular cartilage, sclerosis, and eburnation of subchondral bone, osteophytes and subchondral cysts' (Keuttner and Goldberg 1995). • It is also known as degenerative arthritis, degenerative joint dx, arthritis deformans • Risk factors include advanced age (60 years and above), obesity, e.t.c • Both men and women are affected; the order of affectation in men- hip(most common), knee, spine, ankle, shoulder, fingers; in women- knee, finger, spine, hip, ankle and shoulders CLASSIFICATION

• There are two (2) types of OA- primary and secondary. • Primary (or Generalised) OA is due to no obvious cause • Secondary OA arises as a result of other conditions, such as: 1. Trauma- after severe injury, resulting in fractures (#s) of the joint surfaces 2. Dislocation- this could be (a)repeated minor trauma (b)occupational e.g. miners- knees are at risk, tailors- MCP joints, drillers- elbows and shoulders, etc 3. Infection: (a)tracking into a joint from an open wound (b)tuberculosis of a joint 4. Deformity 5. Obesity 6. Haemophilia 7. Acromegaly 8. Hyperthyroidism 9. Tabes dorsalis, syringomyelia- Charcot’s joints OA- Distribution by Joints AETIOLOGY • Aetiology is unknown but predisposing factors are as follows: 1. Poor posture 2. Ageing process in joint cartilage 3. Heredity: significantly higher incidence in families affected 4. Conditions mentioned in relation to secondary arthritis 5. Defective lubricating mechanism and uneven nutrition of the articular cartilage 6. Climate- this does not cause pathological changes, but pain is greater in cold, dark climates 7. Crystals- calcium pyrophosphate and hydroxyapatite have been associated with synovitis in osteoarthritic joints PATHOLOGY

• Pathology will be considered in relation to each joint structure as follows: 1. Articular cartilage 2. Bone 3. Synovial membrane 4. Capsule 5. Ligaments 6. Muscles Articular hyaline cartilage • In articular cartilage an equilibrium • Another important source of nutrition exists between damage and repair. An occurs during joint loading, when upset of this equilibrium is results in synovial fluid is forced into the negative consequences. cartilage matrix. • Adult articular hyaline cartilage has no • Articular cartilage consists of 10% blood, lymph or nerve supply. chondrocytes, up to 10% • Articular cartilage can be compressed proteoglycans, 10-30% type 2 to one-fifth (20%) its original thickness collagen, 50-70% water, salts, lipids during weight-bearing, so nerves and and other substances such as types iii, blood vessels cannot exist within it vi, ix, x xi, xii and xv collagen. since they would be crushed when the • When a joint is loaded, water is cartilage is compressed. squeezed out of the cartilage matrix. • Its only source of nutrition is synovial This pushes the proteoglycans closer fluid which washes across the surfaces together, making it more resilient to of the joint during movement, further deformation. When the load is providing nourishment. This is known removed, the cartilage absorbs water as synovial sweep. and returns to its resting shape. Articular hyaline cartilage • Fibrillation- or minute cracks and loss of water content occur which lead to softening, splitting and fragmentation of the cartilage. This occurs in both weight-bearing and non-weight- bearing areas of the joint surfaces. • Collagen fibres split and there is a disorganisation of the normal proteoglycan- collagen relationship. As a result, water is attracted into the cartilage matrix, causing further softening and flaking. • These flakes of cartilage break off, float freely within the joint, and may be impacted between the joint surfaces causing locking, inflammation, and synovial irritation. • Proliferation occurs at the periphery of the cartilage and chondrocytes attempt damage repair, but the final product is not as resilient to stress as the original cartilage was. • This sets off a cascade of pathological processes in other tissues. Bone- Pathology in OA • In OA there is a degree of bony remodeling and attempts at repair. This remodeling can be seen in subchondral bone, which becomes eburnated (ivory-like and polished) and on X-ray takes on a white, dense, sclerotic appearance. • The bone ends become hard and abnormally dense, as protection from the overlying cartilage is lost. Cysts may form in the subchondral bone and because eburnated bone is brittle, micro fractures occur, allowing the passage of synovial fluid into the deeper bone. • Venous congestion occurs in the subchondral bone, and osteophytes (bony spurs) form at the margins of the articular surfaces where they may project outwards or into the joint, capsule and ligaments causing sharp stabbing pains. If osteophytes are large enough they cause a mechanical obstruction to joint movement. • Osteophytes are useful to a joint in the sense that they may increase the load-bearing area of a joint, dissipating pressure, but more often they cause problems since they restrict joint movement and are themselves liable to cause pain if nipped. • Bone of the weight-bearing joints alters in shape. Synovial membrane- Changes in OA

• Synovial membrane undergoes hypertrophy and becomes oedematous. • The numerous tiny flakes of cartilage which have broken off act as an irritant to the synovial membrane, and cause repeated effusions. Joint capsule, Ligaments and Muscles- changes in OA

• Capsule- It undergoes fibrous degeneration, adaptive shortening and there are low-grade inflammatory changes. • Ligaments- they undergo same changes as capsule, and become contracted or elongated, depending on the aspect of the joint affected. • Muscles- they may undergo atrophy, which may be related to disuse because pain limits movement and function. Without exercise, the muscles may undergo fibrous atrophy. Clinical Features Related to Pathology

• Pain NB: • Heat • Discussion of the clinical features with • Swelling/joint effusion contribution from the students. • Muscle atrophy and weakness • Loss of movement • Joint stiffness • Muscle spasm • Joint instability • Deformity • Loss of function • Crepitus Clinical Features • Pain: Pain in OA is caused by a cascade of • Stiffness: Stiffness is present after rest and events, ranging from indirect damage to the takes a little time to wear off with cartilage and other synovial joint movement. Stiffness refers to the components. (NB: Pain will be discussed in impairment of quality of movement, not greater detail subsequently). quantity. It may be due to loss of joint • Heat: Superficial joints such as the knee can lubrication, chronic oedema in the become warm to palpation, signifying active periarticular structures, swelling of the inflammation. This cannot always be articular cartilage, or possibly the detected in the deeper joints such as the hip accumulation of hyaluronate in the capsule joint. and synovium. • Loss of joint movement: This is due to • Swelling/joint effusion: Effusion is swelling adaptive soft-tissue shortening or confined to a synovial cavity. 'Swelling' is a lengthening, alteration of joint contour, or more general term. osteophytes. This is different from stiffness • Muscle atrophy/weakness: Either through because it does not wear off. It may be disuse or because of pain inhibition, muscles permanent where there is destruction of become atrophied and weak, often on the articular cartilage, but responds to aspect of the joint that is opposite to physiotherapy if due to muscle spasm or contractures (e.g. the hip extensors are weak contracture of soft tissues. in cases of hip flexion deformity). Clinical Features • Spasm: Spasm is a protective mechanism. • Loss of function: Pain, muscle weakness Movement causes pain so the body and giving way all lead to inability to use attempts to stop movement. Prolonged the joint normally. The pathology of loss spasm causes pain due to metabolite of function is a combination of other accumulation, and fatigue itself may limit clinical features. Each joint adopts a joint movement. It may also interfere characteristic deformity or restriction of with sleep. Adaptive shortening of movements, known as the capsular muscles may also occur (e.g. hamstrings pattern. The capsule of a joint affected by if the knee is held in flexion for prolonged osteoarthritis over a prolonged period periods). behaves in a predictable way, based on • Joint Instability: Loss of proprioception, the affectation. Movements are lost in a loss of ligamentous control, and loss of classical pattern as the joint capsule adequate pressure within the joints as a contracts. result of effusions all contribute to joint • Crepitus: Crepitus can range from mild instability in OA. creaking (which may also indicate synovitis), to loud cracking sounds in • Deformity: Each joint adopts a advanced disease. The flaked cartilage characteristic deformity. and eburnated bone ends grate against each other with a characteristic sound on movement. References

• Bellamy N, Carr A, Dougados M, Shea B, Wells G (2001). Towards a definition of 'difference' in osteoarthritis. Journal of Rheumatology 28: 427-30 • Dandy DJ, Edwards DJ (1998) Essential Orthopaedics and Trauma, 3rd edition. Churchill Livingstone: New York • Lozada CJ, Altaian RD (2001) In: Koopman WJ (ed.) Arthritis and Allied Conditions: a Textbook of Rheumatology. Lippincott Williams & Wilkins: Philadelphia